The highlights of our study on the molecular mechanism of tumor reversion using mouse neuroblastoma cell system as a model during 1983 to 1984 are: (1) We have characterized the polyamine transporter system in mouse neuroblastoma cells. Our studies indicated that this transporter system is Na+-dependent, sensitive to ionophores, and sulfhydryl reagents. The polyamine transporter is also subject to adaptive regulation. More interestingly, we have found that the activity of the transporter can be stimulated by System A amino acids, particularly asparagine. Specific polyamine antimetabolites such as alpha-difluoromethyl ornithine (DFMO), alpha-fluoromethyl ornithine (FMO), and methylglyoxal bis (guanylhydranzone) (MGBG) increase the activity of the polyamine transporter, suggesting that inhibition of polyamine transport should be considered as an integral part in designing effective chemotherapeutic modality aimed at suppressing cellular polyamine content. (2) We have identified the insulin receptor on the cell surface of mouse neuroblastoma cells. We have further demonstrated that there was a 5-fold increase of the insulin-binding sites per cell in the differentiated mouse neuroblastoma cells as compared to the undifferentiated cells. The physiological significance of insulin receptor on mouse neuroblastoma cell surface is currently under investigation. (M)